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Cited by 21PI3K/AKT/mTOR signaling in cancerMetabolism, Diabetes, and CancerHyperglycemia and glycemic control in critically ill and hospitalized patients

The DOI matches its Crossref record; 70 of the 73 references it cites were found in a registry or an index.

A targeted approach to phosphoinositide-3-kinase/Akt/mammalian target of rapamycin-induced hyperglycemia

Cheung, Yee-Ming Melody, McDonnell, Marie, Hamnvik, Ole-Petter Riksfjord·2022·Current Problems in Cancer
DOI 10.1016/j.currproblcancer.2021.100776
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Abstract

Phosphoinositide-3-kinase/Akt/mammalian target of rapamycin (PI3K/Akt/mTOR) pathway inhibitors are a novel class of antineoplastic agent available for the treatment of various cancers. With improved cancer outcomes and survival, individuals are exposed to these antineoplastic therapies for longer periods of time and therefore, the consideration of adverse effects is of increasing importance. The PI3K/Akt/mTOR signaling pathway plays a critical role in regulating cellular processes such as growth and proliferation, but also regulates the metabolic effects of insulin such as glucose uptake and glycogen synthesis. Therefore, hyperglycemia and insulin resistance are frequently reported adverse effects. There are no recent consensus guidelines on the management of hyperglycemia secondary to PI3K/Akt/mTOR inhibitors, with the latest guidelines produced in 2012 - when many of these agents were still undergoing development. As we now have a greater understanding of the underlying mechanisms and patterns in which hyperglycemia is induced and access to an increasing array of glucose-lowering agents, an update of the previous guidelines accommodating these understandings and developments is timely. This review will provide a comprehensive summary of the current literature with regards to the incidence of hyperglycemia associated with each agent, as well as the different pathways and mechanisms in which hyperglycemia is induced. Our proposed up-to-date strategy for the specific managemen…

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Crossref · 10.1016/j.currproblcancer.2021.100776

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Research works printed but not linked: 4

  1. 2021, American Diabetes Association. 2. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes—2021, Diabetes Care, 44 (Supplement 1), S15
  2. André, 2019, Piqray [package insert]. East Hanover, NJ: Novartis Pharmaceuticals Corp;, N Engl J Med, 380, 1929, 10.1056/NEJMoa1813904 · DOI · Paper page
  3. 2021, American Diabetes Association. 12. Older Adults: Standards of Medical Care in Diabetes—2021, Diabetes Care, 44 (Supplement 1), S168
  4. Rugo, 2018, J Clin Oncol, 36

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Metadata

Authors
Cheung, Y.-M. M., McDonnell, M., & Hamnvik, O.-P. R.
Affiliations
Brigham and Women's Hospital (US)
Corresponding author
Hamnvik, Ole-Petter Riksfjord
ORCID
Venue
Current Problems in Cancer
Publisher
Elsevier BV
Published
2022-02
Volume
46
Issue
1
Pages
100776
ISSN
0147-0272 (ISSN-L)
DOI
10.1016/j.currproblcancer.2021.100776
OpenAlex
W3183293567
Cited by
21
References
73
Citations by year
2026: 4 · 2025: 6 · 2024: 4 · 2023: 2 · 2022: 4
FWCI
0.29
Type
journal article
Language
en
Open access
closed
Licence
Locations
  • Current Problems in Cancer (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Hyperglycemia and glycemic control in critically ill and hospitalized patients
Keywords
PI3K/AKT/mTOR inhibitors, hyperglycemia, insulin resistance, antineoplastic drug adverse effects, glucose-lowering agents, hyperglycemia management, glucose metabolism, insulin signaling
MeSH terms
Phosphoinositide-3 Kinase Inhibitors, Antineoplastic Agents, Humans, Hyperglycemia, Neoplasms, Phosphatidylinositols, Phosphatidylinositol 3-Kinases, Sirolimus, Protein Kinase Inhibitors, Proto-Oncogene Proteins c-akt, Phosphatidylinositol 3-Kinase, TOR Serine-Threonine Kinases

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